Researchers have found that a lack of iron during the teen years can have a negative impact on the brain years later, setting the stage for disorders such as Alzheimer’s.
Paul Thompson, a neurology professor at the University of California, Los Angeles, measured levels of transferrin, a protein that transports iron throughout the body and brain, in adolescents and discovered that these levels were related to differences in the brain’s structure when the adolescents reached young adulthood.
“We found that healthy brain wiring in adults depended on having good iron levels in your teenage years,” said Thompson.
“This connection was a lot stronger than we expected, especially as we were looking at people who were young and healthy — none of them would be considered iron-deficient. We also found a connection with a gene that explains why this is so. The gene itself seems to affect brain wiring, which was a big surprise.”
Iron and the proteins that transport it are critically important for brain function, he said. Iron deficiency is the most common nutritional deficiency worldwide, causing poor cognitive achievement in children.
Later in life, too much iron is associated with damage to the brain, and abnormally high concentrations of iron have been found in the brains of patients with Alzheimer’s, Parkinson’s and Huntington diseases.
Since both a deficiency and an excess of iron can negatively impact brain function, the body’s regulation of iron transport to the brain is crucial, according to the researchers. When iron levels are low, the liver produces more transferrin for increased transport.
The researchers wanted to know whether brain structure in healthy adults was also dependent on transferrin levels.
They began by collecting brain MRI scans on 615 healthy twins and siblings, who had an average age of 23. Of these subjects, 574 were also scanned with a type of MRI called a “diffusion scan,” which maps the brain’s myelin connections and their strength, or integrity.
Myelin is the fatty sheath that coats the brain’s nerve axons, allowing for efficient conduction of nerve impulses. Iron plays a key role in myelin production, the researchers note.
Eight to 12 years before the current imaging study, researchers measured the subjects’ blood transferrin levels. They hoped to determine whether iron availability in the developmentally crucial period of adolescence impacted the brain later in life. By averaging the subjects’ transferrin levels, which had been assessed at 12, 14 and 16 years of age, the researchers estimated iron availability to the brain during adolescence, he said.
The team discovered that subjects who had elevated transferrin levels — a common sign of poor iron levels in a person’s diet — had structural changes in brain regions that are vulnerable to neurodegeneration. Further analyses of the twins in the study revealed that a common set of genes influences both transferrin levels and brain structure.
One of the genetic links — a specific variation in a gene called HFE, which is known to influence blood transferrin levels — was associated with reduced brain-fiber integrity, although subjects carrying this variant did not yet show any symptoms of disease or cognitive impairment.
“This is one of the deep secrets of the brain,” Thompson said. “You wouldn’t think the iron in our diet would affect the brain so much in our teen years. But it turns out that it matters very much. Because myelin speeds your brain’s communications, and iron is vital for making myelin, poor iron levels in childhood erode your brain reserves which you need later in life to protect against aging and Alzheimer’s.
“This is remarkable, as we were not studying iron-deficient people, just around 600 normal healthy people,” he continued. “It underscores the need for a balanced diet in the teenage years, when your brain’s command center is still actively maturing. ”
The findings, which appear in the current online edition of the journal Proceedings of the National Academy of Sciences, may aid future studies of how iron transport affects brain function, development and the risk of neurodegeneration, he concluded.